Cardiovascular comorbidities and cardiotoxicity as mechanisms for disparities in treatment outcomes for pediatric Acute Myeloid Leukemia
Mentor Name: Kelly Getz
Cardiac toxicity is a common consequence of the intensive anthracycline-based chemotherapy regimens responsible for dramatic improvements in childhood cancer cure rates. Given that treatment for pediatric acute myeloid leukemia (AML) involves the highest cumulative doses of anthracyclines among all pediatric cancers, these patients are at particularly high risk for the associated short- and long-term cardiac morbidity and mortality. A recent study of de novo pediatric AML therapy demonstrated a >20% incidence of left ventricular systolic dysfunction within one year of treatment. Those with LVSD had a dramatic reduction in both event free and overall survival (OS). Unfortunately, there is a dearth of information on the natural history of cardiotoxicity in pediatric AML, meaningful predictors of its occurrence, and the utilization and effectiveness of cardiac-directed pharmacotherapies in preventing or treating the toxicity. This knowledge gap is likely the result of the limited relevant data captured as part of cooperative group oncology trials. This project aims 1) to determine whether changes in hemodynamics, plasma glucose, and serum creatinine over the duration of AML treatment are associated with changes in left ventricular systolic function and 2) to identify disparities in off-therapy echo monitoring, early incident chemotherapy associated LVSD, and evaluate their role as intermediates in disparities in survival outcomes.
